Size effects of latex nanomaterials on lung inflammation in mice.
Effects of nano-sized materials (nanomaterials) on sensitive population have not been well elucidated. This study examined the effects of pulmonary exposure to (latex) nanomaterials on lung inflammation related to lipopolysaccharide (LPS) or allergen in mice, especially in terms of their size-dependency. In protocol 1, ICR male mice were divided into 8 experimental groups that intratracheally received a single exposure to vehicle, latex nanomaterials (250 microg/animal) with three sizes (25, 50, and 100 nm), LPS (75 microg/animal), or LPS plus latex nanomaterials. In protocol 2, ICR male mice were divided into 8 experimental groups that intratracheally received repeated exposure to vehicle, latex nanomaterials (100 microg/animal), allergen (ovalbumin: OVA; 1 microg/animal), or allergen plus latex nanomaterials. In protocol 1, latex nanomaterials with all sizes exacerbated lung inflammation elicited by LPS, showing an overall trend of amplified lung expressions of proinflammatory cytokines. Furthermore, LPS plus nanomaterials, especially with size less than 50 nm, significantly elevated circulatory levels of fibrinogen, macrophage chemoattractant protein-1, and keratinocyte-derived chemoattractant, and von Willebrand factor as compared with LPS alone. The enhancement tended overall to be greater with the smaller nanomaterials than with the larger ones. In protocol 2, latex nanomaterials with all sizes did not significantly enhance the pathophysiology of allergic asthma, characterized by eosinophilic lung inflammation and Igs production, although latex nanomaterials with less than 50 nm significantly induced/enhanced neutrophilic lung inflammation. These results suggest that latex nanomaterials differentially affect two types of (innate and adaptive immunity-dominant) lung inflammation.
Inoue
Ken-ichiro
K
Environmental Health Sciences Division, National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan. inoue.kenichirou@nies.go.jp
Takano
Hirohisa
H
Yanagisawa
Rie
R
Koike
Eiko
E
Shimada
Akinori
A
D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000276:immunology; D018932:Chemokine CCL2 / Q000187:drug effects / Q000378:metabolism; D016207:Cytokines / Q000187:drug effects / Q000378:metabolism; D004804:Eosinophils / Q000187:drug effects / Q000378:metabolism; D005340:Fibrinogen / Q000187:drug effects / Q000378:metabolism; D007109:Immunity / Q000276:immunology; D007113:Immunity, Innate / Q000276:immunology; D007136:Immunoglobulins / Q000187:drug effects / Q000378:metabolism; D007249:Inflammation / Q000139:chemically induced* / Q000276:immunology; D007840:Latex / Q000633:toxicity*; D008070:Lipopolysaccharides; D008168:Lung / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D049329:Nanostructures / Q000633:toxicity*; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism; D010047:Ovalbumin; D010316:Particle Size; D014841:von Willebrand Factor / Q000187:drug effects / Q000378:metabolism
D018932:Chemokine CCL2; D016207:Cytokines; D007136:Immunoglobulins; D007840:Latex; D008070:Lipopolysaccharides; D014841:von Willebrand Factor; D005340:Fibrinogen; D010047:Ovalbumin